EFFECTS OF DOPAMINE ON POSTURAL CONTROL IN PARKINSONIAN SUBJECTS: SCALING,
SET AND TONE.
Horak, F.B., Frank, J. and Nutt, J.
R.S. Dow Neurological Sciences Institute, 1120 N.W. 20th Avenue, Portland,
OR, USA 97209, Department of Kinesiology, University of Waterloo, Waterloo,
Ontario, Canada N2L 3G1, Department of Neurology, Oregon Health Sciences
University, 3181 S.W. Sam Jackson Park Rd., Portland, OR, USA 97201.APStracts 3:0006N, 1996.
SUMMARY AND CONCLUSIONS
1. This study investigates the effects of parkinsonism and of dopamine
replacement therapy (levodopa) on scaling the magnitude of automatic postural
responses based on sensory feedback and on predictive central set. Surface
reactive torques and electromyographic (EMG) activity in response to backward
surface translations were compared in patients with parkinsonism ON and OFF
levodopa and in elderly control subjects. Correlations between the earliest
postural responses (initial rate of change of torque and integrated EMG) and
translation velocity provided a measure of postural magnitude scaling using
somatosensory feedback. Correlations of responses with expected translation
amplitude provided a measure of scaling dependent upon predictive central set
because the responses preceded amplitude completion. 2. Parkinsonian EMG
responses in six leg and trunk muscles were not later than in elderly control
subjects. In fact, quadriceps antagonist latencies were earlier than normal
resulting in coactivation at the knee not present in control subjects. EMG
activation was fragmented with short burst durations and high tonic levels
which often returned to baseline with multiple bursts. In addition,
parkinsonian responses showed smaller than normal agonist extensor bursts and
larger than normal activation in tibialis and rectus femorus antagonist
flexors. 3. Although parkinsonian subjects scaled postural responses to both
displacement velocities and amplitudes, their torque response were smaller
than that of elderly controls, especially in response to the largest
displacement amplitudes. The gain (slope) of postural response magnitude
scaling to displacement velocity was similar for parkinsonian and control
subjects although parkinsonian subjects had smaller torques. Parkinsonian
subjects were also able to use prediction to scale responses to small expected
displacement amplitudes, but many patients did not generate the larger
plantarflexion torques required at larger displacement amplitudes. Reduced
torque at large amplitudes was associated with less agonist gastrocnemius IEMG
and increased tibialis antagonist burst response and increased tibialis tonic
background activity . 4. Levodopa further reduced the already low magnitude of
initial torque and IEMG responses to displacement velocities and amplitudes in
parkinsonian patients. The ability to scale postural response to velocity
feedback was not affected by Levodopa, but the ability to scale responses to
large displacement amplitudes based on central set was worsened by Levodopa.
Levodopa also significantly reduced the tonic, background levels of EMG,
particularly the distal gastrocnemius and tibialis activity. 5. High baseline
muscle tone was apparent in parkinsonian subjects from their high background
EMG activity in quiet stance, especially in tibialis and quadriceps, and the
slow initial velocity of center of mass falling in response to displacements.
By reducing tone, levodopa reduced passive stiffness to perturbations without
increasing EMG burst magnitudes resulting in less resistance to external
displacements and thus, faster CoM displacements. 6. The biggest postural
deficit in parkinsonian subjects was not in response latency, pattern, or in
reactive or predictive scaling of response magnitude but in quickly generating
an adequate level of postural force. Dopamine improved tonic background
postural tone but further weakened automatic postural responses to external
displacements. Thus, the basal ganglia may participate in postural control by
regulating appropriate levels of background postural tone and by enabling
adequate force generation for resisting external displacements.

Received 17 April 1995; accepted in final form 11 December 1995.
APS Manuscript Number J256-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96